Cellulose is the most abundant polysaccharide on Earth. It can be obtained from a vast number of sources, e.g. cell walls of wood and plants, some species of bacteria, and algae, as well as tunicates, which are the only known cellulose-containing animals. This inherent abundance naturally paves the way for discovering new applications for this versatile material. This review provides an extensive survey on cellulose and its derivatives, their structural and biochemical properties, with an overview of applications in tissue engineering, wound dressing, and drug delivery systems. Based on the available means of selecting the physical features, dimensions, and shapes, cellulose exists in the morphological forms of fiber, microfibril/nanofibril, and micro/nanocrystalline cellulose. These different cellulosic particle types arise due to the inherent diversity among the source of organic materials or due to the specific conditions of biosynthesis and processing that determine the consequent geometry and dimension of cellulosic particles. These different cellulosic particles, as building blocks, produce materials of different microstructures and properties, which are needed for numerous biomedical applications. Despite having great potential for applications in various fields, the extensive use of cellulose has been mainly limited to industrial use, with less early interest towards the biomedical field. Therefore, this review highlights recent developments in the preparation methods of cellulose and its derivatives that create novel properties benefiting appropriate biomedical applications.

/pdf/cellulose-and-its-derivatives-towards-biomedical-27ynon7ox9.pdf

Cellulose and its derivatives: towards biomedical applications

Glioblastoma (GBM) is the most common primary malignant brain tumor in adults and has an exceedingly low median overall survival of only 15 months. Current standard-of-care for GBM consists of gross total surgical resection followed by radiation with concurrent and adjuvant chemotherapy. Temozolomide (TMZ) is the first-choice chemotherapeutic agent in GBM; however, the development of resistance to TMZ often becomes the limiting factor in effective treatment. While O6-methylguanine-DNA methyltransferase repair activity and uniquely resistant populations of glioma stem cells are the most well-known contributors to TMZ resistance, many other molecular mechanisms have come to light in recent years. Key emerging mechanisms include the involvement of other DNA repair systems, aberrant signaling pathways, autophagy, epigenetic modifications, microRNAs, and extracellular vesicle production. This review aims to provide a comprehensive overview of the clinically relevant molecular mechanisms and their extensive interconnections to better inform efforts to combat TMZ resistance.

/pdf/mechanisms-of-temozolomide-resistance-in-glioblastoma-a-1byu7i9rsv.pdf

Mechanisms of temozolomide resistance in glioblastoma - a comprehensive review.

All-trans retinoic acid is a potent promoter of cellular differentiation processes, which is used in cancer therapy. Glioblastoma spheroid cultures are enriched in tumor-initiating cells, and provide a model to test new treatment options in vitro. We investigated the molecular mechanisms of response to exposure to differentiation-promoting conditions in such cultures. Microarray analyses of five independent cultures showed that after induction of differentiation, inhibitors of transforming growth factor-β/bone morphogenetic protein, Wnt/β-catenin and IGF signaling were upregulated, whereas expression of several microRNAs decreased, particularly that of the miR-17-92 cluster. In primary astrocytic gliomas (n=82), expression of several members of miR-17-92 was significantly higher relative to those of normal brain (n=8) and significantly increased with tumor grade progression (P<0.05). A high-level amplification of the miR-17-92 locus was detected in one glioblastoma specimen. Transfection of inhibitors of miR-17-92 induced increased apoptosis and decreased cell proliferation in glioblastoma spheroids. Mir-17-92 inhibition was also associated with increased messenger RNA (mRNA) and/or protein expression of CDKN1A, E2F1, PTEN and CTGF. The CTGF gene was shown to be a target of miR-17-92 in glioblastoma spheroids by luciferase reporter assays. Our results suggest that miR-17-92 and its target CTGF mediate effects of differentiation-promoting treatment on glioblastoma cells through multiple regulatory pathways.

De-repression of CTGF via the miR-17-92 cluster upon differentiation of human glioblastoma spheroid cultures

Extensive data have shown that Wnt/beta-catenin signaling is associated with various disease pathologies, including an important role in tumorigenesis. Here, we review the regulation of Wnt/beta-catenin signaling in glioma, with particular focus on the expression signatures of the main components in Wnt/beta-catenin signaling, the role of key factors in Wnt/beta-catenin signaling, and crosstalk with other signaling pathways. Finally, we discuss the involvement of microRNAs in Wnt/beta-catenin signaling in glioma. This review reveals new insights into the role of Wnt/beta-catenin signaling in gliomagenesis, and highlights new therapeutic approaches for glioma, based on the modulation of the Wnt/beta-catenin pathway.

Wnt/beta-Catenin Signaling in Glioma

Glioblastoma multiformes (GBMs) are extensively heterogeneous at both cellular and molecular levels. Current therapeutic strategies include targeting of key signaling molecules using pharmacological inhibitors in combination with genotoxic agents such as temozolomide. In spite of all efforts, the prognosis of glioma patients remains dismal. Therefore, a proper understanding of individual molecular pathways responsible for the progression of GBM is necessary. The epidermal growth factor receptor (EGFR) pathway is probably the most significant signaling pathway clinically implicated in glioma. Not surprisingly, anti-EGFR therapies mostly prevail for therapeutic purposes. The Wnt/β-catenin pathway is well implicated in multiple tumors; however, its role in glioma has only recently started to emerge. We give a concise account of the current understanding of the role of both these pathways in glioma. Last, taking evidences from a limited literature, we outline a number of points where these pathways intersect each other and put forward the possibility of combinatorially targeting them for treatment of glioma.

https://gan.sagepub.com/content/4/11-12/427.full.pdf

Current Understanding on EGFR and Wnt/β-Catenin Signaling in Glioma and Their Possible Crosstalk

Adipose-derived stem cells (ADSCs) are multipotent and have received increasing attention for their applications in medicine. Cell-based therapies are optimal for diseases with loss or damage to tissues or organs. ADSCs and bone marrow mesenchymal stem cells (BMSCs) can differentiate into many cell lineages. Because of their advantages in accessibility and volume, ADSCs are regarded as a desirable alternative to BMSCs. In this study, we focused on the chondrocytic differentiation potential of ADSCs and the underlying mechanism. We found that the long noncoding RNA H19 plays an important role in this process. Overexpression of H19 in ADSCs induced differentiation towards chondrocytes. H19 is abundantly expressed during embryonic development and downregulated after birth, implying its regulatory role in determining cell fate. However, in our experiments, H19 exerted its regulatory function during cartilage differentiation of ADSCs through competing miRNA regulation of STAT2.

/pdf/long-noncoding-rna-h19-participates-in-the-regulation-of-gi818hq5vv.pdf

Long Noncoding RNA H19 Participates in the Regulation of Adipose-Derived Stem Cells Cartilage Differentiation

The CIDE genes might serve as novel targets for therapeutic intervention of obesity.

Aim To find a method for isolation and cultivation of human adipose-derived mesenchymal stem cells(ADSCs), and to investigate its chondrogenic ability. Methods Liposuction human adipose tissues were digested with collagenase type II. The obtained cells were primarily cultured in DMEM medium, and then changed into the induced medium. Alcian Blue stain, picrosirius red stain and the specific collagenase type II immunohistochemical staining were used to detect the results. Results After cultured in chondrogenic medium, the cells differentiated toward cartilage cells and secreted the specific cartilaginous matrices sulfated proteglycan and collagen type II. Conclusion The human ADSCs have the potential ability to differentiate toward cartilage cells in the appropriated medium. The result provide a new method for the further research in cartilaginous tissue engineering.

[Isolation, cultivation of adipose-derived mesenchymal stem cells and its chondrogenic ability].

This study demonstrated a newly developed method using adipose tissue-derived stromal cells (ADSCs) and hydroxypropylmethylcellulose (HPMC) in building injectable tissue engineered cartilage in vivo. ADSCs from rabbit subcutaneous fatty tissue were cultured in chondrogenic differentiation medium and supplemented with transforming growth factor-β1 (TGF-β1) and basic fibroblast growth factor (bFGF). Histological, immunohistochemistry and RT-PCR analysis confirmed that the ADSCs differentiated into chondrocytes following induction. Induced ADSCs mixed with 15 % HPMC were injected into the subcutaneous tissue of nude mice and, after a period of 8 weeks, newly formed cartilage was observed at the site of injection. The ability of ADSCs cultured in the induction medium with TGF-β1 and bFGF to differentiate into chondrocytes and construct new cartilage indicates that ADSCs are suitable for use as seed cells in cartilage tissue engineering. HPMC, according to its good water solubility and being able to transform from liquid to solid at body temperature, was found to be an ideal scaffold for tissue engineering.

/pdf/the-role-of-adipose-derived-stromal-cells-and-5gqgfqyfev.pdf

The role of adipose-derived stromal cells and hydroxypropylmethylcellulose in engineering cartilage tissue in vivo

The invention discloses a cartilage tissue engineering scaffold material for injection, which contains 10 to 15 percent hydroxypropyl methylcellulose and cartilage seed cells with a concentration of 5x10 /ml By observing the change of physical characteristics of HPMC with different concentrations under different temperature conditions, the concentration between 10 and 15 percent is selected as the optimum concentration used to form gelatin; during the application, after a compound of the cartilage seed cells and the HPMC is injected into a subcutaneous tissue on the back of a nude mouse, a tissue engineering cartilage can be formed in a body of the nude mouse, and the formed cartilage has the characteristics of cartilage tissues proven by the histology

Cartilage tissue engineering bracket material for injections

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